ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Repurposing lurasidone to alleviate doxorubicin-induced cardiotoxicity and neurotoxicity via BDNF/TrkB/PI3K/Akt/CREB and miR-34a-5p/PGC-1α pathways.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Doxorubicin (Dox) is a potent cytotoxic medication, yet its adverse properties are undeniable obstacles to its clinical use. The objective of the existing research was to inspect the potential beneficial actions of lurasidone (Lura) against the neurotoxicity and cardiotoxicity triggered by Dox in rats. Sixty rats were equally allocated to four groups: Control group; Dox group; Lur (1 mg/kg) + Dox group; Lura (3 mg/kg) + Dox group. For 18 days, Lura (1 and 3 mg/kg) was given orally, starting 7 days before giving six doses of Dox (2.5 mg/kg every other day, i.p). Lura attenuated Dox-instigated cardiac injury as assured by the decrease in cardiac troponin-I (cTn-I), kg) and creatine kinase MB (CK-MB) levels. In addition, Lura remarkably declined Dox-triggered neuronal dysfunction, as confirmed by diminished anxiety and depression-alike behaviors in the open field (OFT) and forced swimming (FST) tests, respectively. Furthermore, Lura replenished cardiac and brain antioxidant markers, mitochondrial modulator, PGC-1α, and significantly decreased inflammatory mediators, miR34a-5p, and pro-apoptotic caspase-3 levels. In the brain, Lura also mitigated the induction of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor-1 (Iba-1). In the same context, Lura pretreatment upregulated the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/phosphoinositide 3-kinase (PI
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